Characterizing the combined effects of force, repetition and posture on injury pathways and micro-structural damage in isolated functional spinal units from sub-acute-failure magnitudes of cyclic compressive loading.

Background: Previous research suggests that when the magnitude of peak compressive force applied during cyclic loading exceeds 30% of a functional spinal unit's estimated ultimate compressive tolerance, fatigue failure of the cartilaginous endplate or vertebra will occur before intervertebral disc herniation.

Methods: Three levels of peak compressive force, three cycle rates and two dynamic postural conditions were examined using a full-factorial design. Cyclic compressive force was applied using a modified material testing apparatus, in accordance with a biofidelic time-varying waveform with synchronous flexion/extension rotation for 5000 cycles.

Phospholamban overexpression in mice causes a centronuclear myopathy-like phenotype.

Centronuclear myopathy (CNM) is a congenital myopathy that is histopathologically characterized by centrally located nuclei, central aggregation of oxidative activity, and type I fiber predominance and hypotrophy. Here, we obtained commercially available mice overexpressing phospholamban (Pln(OE)), a well-known inhibitor of sarco(endo)plasmic reticulum Ca(2+)-ATPases (SERCAs), in their slow-twitch type I skeletal muscle fibers to determine the effects on SERCA function. As expected with a 6- to 7-fold overexpression of phospholamban, SERCA dysfunction was evident in Pln(OE) muscles, with marked reductions in rates of Ca(2+) uptake, maximal ATPase activity and the apparent affinity of SERCA for Ca(2+).

Autophagic signaling and proteolytic enzyme activity in cardiac and skeletal muscle of spontaneously hypertensive rats following chronic aerobic exercise.

Hypertension is a cardiovascular disease associated with deleterious effects in skeletal and cardiac muscle. Autophagy is a degradative process essential to muscle health. Acute exercise can alter autophagic signaling.

High-fat feeding does not induce an autophagic or apoptotic phenotype in female rat skeletal muscle.

Apoptosis and autophagy are critical in normal skeletal muscle homeostasis; however, dysregulation can lead to muscle atrophy and dysfunction. Lipotoxicity and/or lipid accumulation may promote apoptosis, as well as directly or indirectly influence autophagic signaling. Therefore, the purpose of this study was to examine the effect of a 16-week high-fat diet on morphological, apoptotic, and autophagic indices in oxidative and glycolytic skeletal muscle of female rats.

Autophagy is required and protects against apoptosis during myoblast differentiation.

Several degradative systems assist in formation of multinucleated terminally differentiated myotubes. However, the role of autophagy in this process has not been examined. GFP-LC3B (light chain 3 beta) puncta, LC3B-II protein and LysoTracker fluorescence increased during C2C12 cell differentiation.

Glucopsychosine increases cytosolic calcium to induce calpain-mediated apoptosis of acute myeloid leukemia cells.

To identify novel anti-cancer agents, we created and screened a unique nutraceutical library for activity against acute myeloid leukemia (AML) cells. From this screen, we determined that glucopsychosine was selectively toxic toward AML cell lines and primary AML patient samples with no effect toward normal hematopoietic cells. It delayed tumor growth and reduced tumor weights in mouse xenograft models without imparting toxicity.

Potentiation in mouse lumbrical muscle without myosin light chain phosphorylation: is resting calcium responsible?

The increase in isometric twitch force observed in fast-twitch rodent muscles during or after activity, known universally as potentiation, is normally associated with myosin regulatory light chain (RLC) phosphorylation. Interestingly, fast muscles from mice devoid of detectable skeletal myosin light chain kinase (skMLCK) retain a reduced ability to potentiate twitch force, indicating the presence of a secondary origin for this characteristic feature of the fast muscle phenotype. The purpose of this study was to assess changes in intracellular cytosolic free Ca(2+) concentration ([Ca(2+)](i)) after a potentiating stimulus in mouse lumbrical muscle (37°C).

Decreased DNA fragmentation and apoptotic signaling in soleus muscle of hypertensive rats following 6 weeks of treadmill training.

Cardiovascular diseases such as hypertension are associated with a generalized skeletal myopathy including a proapoptotic phenotype. Current evidence suggests that exercise may alter apoptosis-related signaling in skeletal muscle; however, the effect of exercise on skeletal muscle DNA fragmentation and apoptotic signaling is unclear in hypertensive animals. Male normotensive Wistar Kyoto (WKY; n = 24) and spontaneously hypertensive rats (SHR; n = 24) were assigned to a sedentary (SED) condition or exercise (EX) consisting of progressive treadmill running 5 days/wk for 6 wks.

Exercise is an effective treatment modality for reducing cancer-related fatigue and improving physical capacity in cancer patients and survivors: a meta-analysis.

The use of exercise interventions to manage cancer-related fatigue (CRF) is a rapidly developing field of study. However, results are inconsistent and difficult to interpret across the literature, making it difficult to draw accurate conclusions regarding the true effectiveness of exercise interventions for CRF management. The aims of this study were to apply a meta-analysis to quantitatively assess the effects of exercise intervention strategies on CRF, and to elucidate appropriate exercise prescription guidelines.

Differential apoptosis-related protein expression, mitochondrial properties, proteolytic enzyme activity, and DNA fragmentation between skeletal muscles.

Increased skeletal muscle apoptosis has been associated with a number of conditions including aging, disuse, and cardiovascular disease. Skeletal muscle is a complex tissue comprised of several fiber types with unique properties. To date, no report has specifically examined apoptotic differences across muscles or fiber types.